This review explains that the antimicrobial peptide LL‑37, which normally helps fight infections, can also trigger inflammation in psoriasis by forming complexes with DNA that activate immune cells, especially the Th17/IL‑23 pathway. It highlights that LL‑37 is a key link between innate immunity and the skin disease.

Antimicrobial peptides (AMPs) are a group of oligopeptides found in most multicellular organisms with a capacity for rapid and nonspecific destruction of pathogens. The action of destroying pathogens is associated with a strong proinflammatory activity, stimulating the secretion of cytokines, chemokines, growth factors but also chemotaxis, the activation of dendritic cells and involving adaptive immunity also. The action of AMPs fits perfectly into the characteristics of innate immunity which makes these peptides candidates to be considered as an important element of this type of immunity. It has been shown that AMPs are involved in a number of cellular processes such as: differentiation, proliferation, maturation, thus widening the degree of involvement of these peptides in the pathogenesis of chronic inflammatory diseases. In psoriasis, AMPs act both as a pro-inflammatory and chemotaxis factor and through the cathelicidin (LL-37)/dc DNA complex as a possible autoantigen for T cells, triggering an autoimmune response, activating the Th17/IL23 axis and maintaining the inflammatory process. Thus, many arguments are accumulated to consider that innate immunity through AMPs is an important link in the pathogenesis of psoriasis. Moreover, the action of antimicrobial peptides in psoriasis is almost entirely characteristic for the general mode of action of innate immunity.